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Epidemic dropsy and the Ocular Manifestations

Dr. S.K. Narang MS. Senior President Eye Department E.S.I. Hospital Basaidarapur.

Dr. R.S.D. Sachdeva MS. Head of the Eye Department E.S.I. Hospital Basaidarapur.

Dr. K.A. Ramakrishnan MD. Head of the Medicine Department E.S.I. Hospital Basaidarapur.

Introduction

Epidemic dropsy was first registered in 1877 when it appeared as an Epidemic dropsy in Calcutta. The cause of Epidemic dropsy was not known until 1836, when Sarkar discribed it to the communication of mustard oil with argemone oil. (Outbreaks of Epidemic dropsy have been frequently noted in India in states of West Bengal, Uttar Pradesh, Orissa, Bihar, Madhya Pradesh and Delhi. Mustard oil is a common cooking medium in these parts and ingestion of contaminated mustard oil message over the body can result in significant absorption produce disease. The disease has been recorded in Fizi, Mauritious and South Africa among Indian emigrants who have persisted with their original dietetic habits.

The contamination of mustard or other oil like graundnut, arachis and vanaspati, with argemone oil may be accidental or deliberate. Seeds of argemone mexicana (Prickly poppy) closely resemble mustard seeds. The plant grows wild in India. It has prickly leaves and bright yellow flowers. Crops of mustard are gathered during March and during the period, the seeds of argemone also mature and are likely to be harvested alongwith mustard seeds. The other way, the disease can be caused is by adulterating black mustard seeds by the unscruplous traders with seeds of argemone mexicana which are also black in colour. Argemone oil may similarly be mixed with mustard oil, the former being much cheaper. Argemone seed oil contains two physiologically active benzophenanthridine toxic alkaloids Sanguinarine and dihhydrosanguinarine.

The disease affects both sexes and all age groups except breast fed infants. There is a seasonal variation in the incidence, peak occuring in July-August when freshly extracted oil is marketed. The incidence is lowest in April and is probably related to the loss of toxicity due to storage of oil.

Etapathogenesis

Argemone mexicana seeds when crushed release toxins sanguinarine and dihydrosanguinarine which like thiamine deficiency states inhibits end stages of carbohydrate metabolism, resulting in accumulation of pyruvic acid in blood. Vascular changes dominate the pathology. These effect skin, mucous membranes, deeper structures, heart muscle and uveal tract. Edema, initially due to increased capillary permeability and later due to cardiac decompensation, affects subcutaneous tissues particularly of the legs. Their may be effusion in the serious cavities. There is generalised acute vasodilation of capillaries and telangiectasis.

Systemic Clinical Features

The disease may occur in epidemic form or as an isolated instance in endemic areas. The onset is usually insidious but may be subacute. The severity of symptoms varies widely. Gastrointestinal symptoms are prominent at the onset. After a few days of anorexia, nausea, flatulence, abdominal pain and watery diarrhoea edema appears on lower limbs. It is a constant feature of the disease, soft and pitting on pressure usually confined to legs, increasing on waling and often resistant to treatment. The edema progresses to other parts producing generalized anasarca. Effusions may occur in pleural, pericardial and peritonial cavities. In severe cases, cardiac decompensation occurs gradually or rapidly and dyspnoea at rest worsening on exertion dominates the clinical picture. In patients with cardiac involvement the electrocardiogram shows non specific St. T segment and T wave changes. The rythem may be regular with sinus tachycardia or irregular due to extrasystoles or atrial fibillation. The latter may precipitate acute heart failure with enlarged tender liver and pulmonary edema which may be fatal. There may be bronichitis and bronchopneumonia.

Dilatation of peripheral blood vessels imparts irregularly mottled reddish appearance to the skin of the edematous lower limbs. Such irregularly formed new vessels in the skin produce nodular haemangiomata so called `saccoids' which may be infected and ulcerated, bleeding readily when injured. Some patients may be mildly febrile.

Ocular Manifestations in Epidemic dropsy

Epidemic Dropsy came to the attention of ophthalmologists only in 1909 when Maynard reported the occurrence of glaucoma in some cases of the disease. Ocular manifestations in most of the patients are a relatively feature of the disease. Main ocular manifestations of epidemic dropsy can be listed as under:

* Glaucoma

* Sub conjunctival haemorrhages

* Fundus Changes

__ Dilatation with or without tortuosity of vessels

__ Superficial retinal haemorrhages

__ Microaneurysms

__ Disc edema

__ Peripapillary edema

Glaucoma

Glaucoma is independent of the severity of the systemic features and retinal vascular changes and develop in cases with long standing disease. Raised intraocular pressure is associated with wide diurnal swings. Glaucoma as a rule is bilateral with open angles, a normal chamber depth and no signs of anterior segment inflammation. The outflow facility is unimpaired. No clinically significant cup-disc changes are seen in early cases although in long standing cases cup-disc ratio may be increased and even glaucomatous optic drophy may be seen. Similarly perimetry also does not reveal any field defects in early stages. During later stages, glaucomatous field defects may be present. Glaucoma is more commonly seen in younger age groups. The incidence of glaucoma in various epidemics ranges from 0-12%.

Dropsy glaucoma is hypersecretary in nature associated with increased aqueous production. This is due to increased vascular permeability of the ciliary processes caused by the toxins sanguinarine and dihydrosanguinarine. The prostaglandins and histamine have also been implicated in the causation of dropsy glaucoma.

Regarding treatment drugs which primarily reduce aqueous production have a beneficial effect. Various such drugs are timolol maleate, epinephrine (1% or 2%), dipivefrin hydrochloride (0.1%), acetazolamide. Systemic or topical nonsteroidal antiflammatory drugs especially indomethacin and topical steroids by virtue of their antiprostaglandin activity lead to normalisation of increased vascular permeability of ciliary body and a consequent reduction in aqueous production and intra ocular pressure. Topical Clonidine a centrally acting drug also has a role in dropsy glaucoma management. Drugs which have a primary effect on the outflow channels like pilocarpine are ineffective. Multi drug therapy for prolonged periods should be used since the glaucoma is self limited. Trabeculectomy should only be done when maximal medical therapy fails.

Sub conjunctival haemorrhage

Sub conjunctival haemorrhage is also due to dilatation and increased permeability of vessels.

Fundus Changes

Fundus picture which reflects systemic status of the patient has no correlation with glaucoma. The fundus examination basically reveals venous stasis like picture. The changes seen are as under:

* Venous dilatation and torousity is the commonest abnormality seen, being proportionate to the severity of systemic problem. This is due to intense non inflammatory capillary dilatation.

* Superficial retinal haemorrhages are also common seen and are scattered mainly over the posterior pole but are also present in areas anterior to equator. They are usually associated with cardiovascular decompensation. Retinal haemorrhages are due to toxic vasculitis, venous stasis and anemia which is present in most of the cases. Superficial retinal haemorrhages usually resolve first taking about one to four weeks whereas venous tortuosity and dilatation take about four to eight weeks to disappear.

* Disc edema seen in some patients is due to intense noninflammatory capillary dilatation. This is usually associated with peripapillary edema. Most of the patients with disc edema have cardiovascular decompensation which progresses to congestive cardiac failure with a high mortality. It can later on result in secondary optic atrophy.

* Microaneurysms if present are also due to noninflammatory capillary dilatation.

* Pigmentary changes in the form of hypo and hyperpigmented stippling around the optic disc and posterior pole and occasionally in the far periphery are also seen.

Fundus examination in dropsy patients can be used to arrive at general and visual prognosis.

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For kind Attention - Dr. Lalit Verma

Epidemic Dropsy and its Secy. DOS

Ocular Manifestations

Total number of patients seen in E.S.I. Hospital, Basaidarapur, N. Dec in Aug. Sept. 1998. 216

Table-I systemic Clinical Features

By lateral pedal oedema 216 (100%)

Gestrointestinal symptoms 195 (90.3%)

Diarrhoea/Nausea/Flatulence

Erythema over Ordematous 160 (74%)

Angioma of Skin 5 (2.3%)

Raised skin temperature 160 (74%)

Mild to moderate anaemia 100 (46.2%)

Congestive Cardiac Failure 30 (13.9%)

Radiological features of pleural effusion 35 (16.2%)

Bleeding persectum 15 (6.9%)

Number of deaths (all fourched of Congestive

Cardiac failure) 4 (1.85%)

Ocular Manifestations

Total number of patients 216

Patients examined in eye department 180

I. Glaucoma Seen in 8 (4.4%)

II. Fundus Changes

A. Dilatation and tortrosity of retinal vein 119 (66.1%)

B. Superficial retinal haemorrhages 40 (22.2%)

C. Dilation and tortuosity of retinal veins with retinal haemorrhages 40 (22.2%)

D. Microancurysm 15 (8.3%)

E. Disc oedema 3 (1.7%)

F. Optic atrophy 0

G. Normal fundus 6

Correlation between ocular and systemic features

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